GU OncologyDr. Saleh Binsaleh

Assistant Professor and Consultant Urologist

Contents Renal Tumors Bladder Tumors Prostate Tumors Testis Tumors

Renal Tumors

Renal Tumors Benign tumours of the kidney are

rare All renal neoplasms should be

regarded as potentially malignant Renal cell carcinomas arise from the

proximal tubule cells

Male : female ratio is approximately 2:1

Increased incidence seen in von Hippel-Lindau syndrome

Pathologically may extend into renal vein and inferior vena cava

Blood born spread can result in 'cannon ball' pulmonary metastases

‘Cannon Ball' Pulmonary Metastases

Clinical features 10% present with classic trial of

haematuria, loin pain and a mass Other presentation include a pyrexia

of unknown origin, hypertension Polycythaemia due to erythropoietin

production Hypercalcaemia due to production of

a PTH-like hormone

Investigations

Diagnosis can often be confirmed by renal ultrasound

CT scanning allows assessment of renal vein and caval spread

Echocardiogram should be considered if clot in IVC extends above diaphragm

Management Unless extensive metastatic disease it

invariably involves surgery Surgical option usually involves a radical

nephrectomy Kidney approached through either a

transabdominal or loin incision Renal vein ligated early to reduce tumour

propagation Kidney and adjacent tissue (adrenal,

perinephric fat) excised

Open Radical Nephrectomy

Laparoscopic Nephrectomy

Rx: Lymph node dissection of no proven

benefit Solitary (e.g. lung metastases) can

occasionally be resected Radiotherapy and chemotherapy

have No role Immunotherapy can help

( Performance status)

Bladder Tumors

Pathology

Of all bladder carcinomas: 90% are transitional cell carcinomas 5% are squamous carcinoma 2% are adenocarcinomas

TCCs should be regarded a 'field change' disease with a spectrum of aggression

80% of TCCs are superficial and well differentiated Only 20% progress to muscle invasion Associated with good prognosis

20% of TCCs are high-grade and muscle invasive 50% have muscle invasion at time of presentation Associated with poor prognosis

Etiological factors Occupational exposure 20% of transitional cell carcinomas are

believed to result from occupational factors

Chemical implicated - aniline dyes, chlorinated hydrocarbons

Cigarette smoking Analgesic abuse e.g. phenacitin Pelvic irradiation - for carcinoma of the

cervix Schistosoma haematobium associated

with increased risk of squamous carcinoma

Presentation 80% present with painless

hematuria Also present with treatment-

resistant infection or bladder irritability and sterile pyuria

Investigation of Painless Haematuria

Urinalysis Ultrasound - bladder and kidneys KUB - to exclude urinary tract

calcification Cystoscopy Urine Cytology Consider IVU if no pathology

identified

IVP

Pathological staging Requires bladder muscle to be included in

specimen Staged according to depth of tumour

invasion Tis In-situ disease Ta Epithelium only T1 Lamina propria invasion T2 Superficial muscle invasion T3a Deep muscle invasion T3b Perivesical fat invasion T4 Prostate or contiguous muscle

Grade of Tumor G1 Well differentiated G2 Moderately well

differentiated G3 Poorly differentiated

Carcinoma in-situ Carcinoma-in-situ is an aggressive

disease Often associated with positive

cytology 50% patients progress to muscle

invasion Consider immunotherapy If fails patient may need radical

cystectomy

Treatment of bladder carcinomas

Superficial TCC Requires transurethral resection and

regular cystoscopic follow-up Consider prophylactic chemotherapy if

risk factor for recurrence or invasion (e.g. high grade)

Consider immunotherapy BCG = attenuated strain of

Mycobacterium bovis Reduces risk of recurrence and

progression 50-70% response rate recorded Occasionally associated with development

of systemic mycobacterial infection

TURBT

Rx: Invasive TCC Radical cystectomy has an operative

mortality of about 5% Urinary diversion achieved by:

Ileal conduit Neo-bladder

Local recurrence rates after surgery are approximately 15% and after radiotherapy alone 50%

Pre-operative radiotherapy is no better than surgery alone

Adjuvant chemotherapy may have a role

Prostate Tumors

Prostate cancer Commonest malignancy of male

urogenital tract Rare before the age of 50 years Found at post-mortem in 50% of men

older than 80 years 5-10% of operation for benign

disease reveal unsuspected prostate cancer

Pathology The tumours are adenocarcinomas Arise in the peripheral zone of the

gland Spread through capsule into

perineural spaces, bladder neck, pelvic wall and rectum

Lymphatic spread is common Haematogenous spread occurs to

axial skeleton Tumours are graded by Gleeson

classification

Clinical features

Majority these days apre picked up by screening

10% are incidental findings at TURP Remainder present with bone pain,

cord compression or leuco-erythroblastic anaemia

Renal failure can occur due to bilateral ureteric obstruction

Diagnosis With locally advanced tumours diagnosis

can be confirmed by rectal examination Features include hard nodule or loss of

central sulcus Transrectal biopsy should be performed Multiparametric MRI maybe useful in the

staging of the disease Bone scanning may detect the presence of

metastases Unlikely to be abnormal if asymptomatic

and PSA < 10 ng/ml

Serum prostate specific antigen (PSA)

Kallikrein-like protein produced by prostatic epithelial cells

4 ng/ml is the upper limit of normal >10 ng/ml is highly suggestive of

prostatic carcinoma Can be significantly raised in BPH Useful marker for monitoring

response to treatment

Treatment More men die with than from prostate cancer Treatment depends on stage of disease, patient's

age and general fitness Treatment options are for: Local disease

Observation Radical radiotherapy Radical prostatectomy

Locally advanced disease Radical radiotherapy Hormonal therapy

Metastatic disease Hormonal therapy

Open

Laparoscopic

Robotic

Brachytherapy

EBRT

EBRT

Hormonal therapy 80-90% of prostate cancers are androgen

dependent for their growth Hormonal therapy involves androgen

depletion Produces good palliation until tumours

'escape' from hormonal control Androgen depletion can be achieved by:

Bilateral orchidectomy LHRH agonists - goseraline Anti-androgens - cyproterone acetate,

flutamide, Biclutamide Complete androgen blockade

Testicular Tumors

Testicular Tumors Commonest presentation: testicular

swelling on the side of the tumor. Commonest malignancy in young men Highest incidence in caucasians in

northern Europe and USA Peak incidence for teratomas is 25 years

and seminomas is 35 years In those with disease localised to testis

more than 95% 5 year survival possible Risk factors include cryptorchidism,

testicular maldescent and Klinefelter's syndrome

Classification Seminomas (~50%) None-Seminoma (~50%)

Teratomas Yolk sac tumours Embryonal Mixed Germ cell yumor

Investigation Diagnosis can often be confirmed by testicular

ultrasound Pathological diagnosis made by performing an

inguinal orchidectomy Disease can be staged by thoraco-abdominal CT

scanning Tumor markers are useful in staging and

assessing response to treatment o Alpha-fetoprotein (alphaFP)

Produced by yolk sac elements Not produced by seminomas

o Beta-human chorionic gonadotrophin (betaHCG) Produced by trophoblastic elements Elevated levels seen in both teratomas and

seminoma o LDH

Stage Definition I Disease confined to testis IM Rising post-orchidectomy

tumour marker II Abdominal lymphadenopathy

A  < 2 cm B 2-5 cm C > 5 cm III Supra-diaphragmatic disease

Seminomas

Seminomas Seminomas are radiosensitive The overall cure rate for all stages of

seminoma is approximately 90%. Stage I and II disease treated by inguinal

orchidectomy plus Radiotherapy to ipsilateral abdominal

and pelvic nodes ('Dog leg') or Surveillance

Stage IIC and above treated with chemotherapy

Radical Orchiectomy

None-Seminoma

None-Seminoma None-Seminoma are not

radiosensitive Stage I disease treated by

orchidectomy and surveillance Vs RPLVD Vs Chemo

Chemotherapy (BEP = Bleomycin, Etopiside, Cisplatin) given to:

Stage I patients who relapse Metastatic disease at presentation

Questions